Thurner · The Journal of pharmacology and experimental therapeutics 2014 · in vitro electrophysiological and molecular modeling study · n=?

Mechanism of hERG channel block by the psychoactive indole alkaloid ibogaine.

Cited 41 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

In vitro electrophysiological and computational modeling study without human participants.

PubMed 24307198 · doi:10.1124/jpet.113.209643 · record verified 2026-08-28

What was done

Researchers investigated the mechanism of human ether-à-go-go-related gene (hERG) potassium channel inhibition by ibogaine. Experiments were conducted using mammalian kidney tsA-201 cells heterologously expressing wild-type or mutated hERG channels (Y652A, F656A, and the inactivation-deficient G628C/S631C double mutant). Electrophysiological recordings evaluated extracellular versus intracellular drug application, pH dependence, voltage dependence, and gating kinetics, complemented by molecular docking and kinetic modeling.

What was found

The abstract reports qualitative mechanistic findings without exact numerical values (such as IC50s or millivolt shifts). Ibogaine blocked hERG channels via both extracellular and intracellular routes, with inhibition extent depending on relative pH. Block occurred during channel activation but spared resting channels, developing faster with increasing depolarization. Ibogaine shifted steady-state activation and inactivation to more negative potentials, slowed deactivation, and accelerated inactivation. Mutations at Y652A and F656A reduced ibogaine potency, whereas G628C/S631C retained wild-type sensitivity. Molecular docking and kinetic modeling confirmed ibogaine binds inside the inner channel cavity preferentially in open and inactivated conformations.

Why it matters

This study provides a direct biophysical explanation for ibogaine-induced QT prolongation and cardiac arrhythmias, identifying specific binding residues and channel states responsible for cardiotoxicity.

Limits

The study was conducted entirely in an engineered in vitro cell culture model and molecular simulations. No in vivo cardiac electrophysiology, whole-heart assays, or clinical human pharmacokinetic/pharmacodynamic data were included, and the abstract omits exact concentrations and quantitative IC50 values.

Cited by